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研究结核杆菌pckA基因编码的磷酸烯醇型丙酮酸羧激酶(PEPCK)诱导机体产生的保护性免疫反应。用敲除pckA基因的牛结核杆菌BCG和野生型BCG分别感染小鼠,取肝、肺、脾进行病理分析,并进行脾细胞培养,检测CD4+、CD4+/CD8+、细胞因子IFNI-γI、L-12和TNF等。用敲除pckA基因的BCG感染的小鼠比野生型BCG感染的小鼠体内产生的结核结节少且不典型,炎性程度低。野生型BCG感染的小鼠脾脏内的CD4+T细胞和CD4+/CD8+、细胞因子IFN-γ、IL-12、TNF均明显高于敲除pckA基因BCG感染的小鼠。pckA基因为结核杆菌生长所必需,其编码产物PEPCK能够刺激机体产生免疫反应,是一种很好的疫苗候选分子。
To study the phosphorylation of phosphoenolpyruvate carboxykinase (PEPCK) encoded by Mycobacterium tuberculosis pckA gene to induce the body’s protective immune response. Mice were infected with BCG knockout pckA gene and wild-type BCG respectively. Pathological analysis was performed on the liver, lung and spleen of the mice and the splenocytes were cultured. The levels of CD4 +, CD4 + / CD8 +, cytokines IFN-? IL- 12 and TNF and so on. Mice infected with BCG that knocked out the pckA gene produced less tubercles than atypical, less inflammatory nodules than wild-type BCG-infected mice. CD4 + T cells and CD4 + / CD8 +, cytokines IFN-γ, IL-12 and TNF in spleen of wild-type BCG infected mice were significantly higher than those in mice infected with BCG infected with pckA gene. The pckA gene is essential for the growth of Mycobacterium tuberculosis, and its encoded product PEPCK can stimulate the body to produce an immune response and is a good vaccine candidate molecule.